白藜芦醇对力竭运动大鼠心肌细胞凋亡影响

Effects of resveratrol on apoptosis of cardiomyocytes in exercise-exhausted rats

目的摘探讨白藜芦醇对力竭运动大鼠心肌细胞氧化应激、凋亡影响及机制。方法成年雄性SD大鼠随机分为5组:对照组、力竭运动组、白藜芦醇50、100、200 mg/kg组,检测大鼠心肌组织缺血缺氧面积、心肌组织超氧化物歧化酶(SOD)、丙二醛、Ca^(2+)-ATPase含量,TUNEL法检测心肌细胞凋亡率,Western blot法检测心肌细胞Bax和caspase-3蛋白表达。结果与对照组比较,力竭运动组大鼠心肌缺血缺氧面积[(112.27±48.27)μm^2]与心肌组织丙二醛含量[(3.98±0.75)nmol/mgpro]明显升高、心肌组织SOD活性[(30.54±4.29)U/mgpro]与Ca^(2+)-ATPase活性[(0.32±0.03)mol/(mg·h)]明显下降、心肌细胞凋亡指数[(23.4±2.3)%]与心肌组织Bax、caspase-3蛋白表达[(1.28±0.32)、(1.59±0.12)]明显升高;与力竭运动组比较,200 mg/kg白藜芦醇组大鼠心肌缺血缺氧面积[(22.12±10.22)μm^2]与心肌组织丙二醛含量[(1.65±0.11)nmol/mgpro]明显减少、心肌组织SOD、Ca^(2+)-ATPase活性[分别为(69.57±9.02)U/mgpro、(0.72±0.11)mol/(mg·h)]明显升高、心肌细胞凋亡指数[(10.4±1.3)%]与心肌组织Bax、caspase-3蛋白表达[(0.36±0.11)、(0.62±0.13)]明显降低(P<0.01);呈明显剂量效应关系。结论白藜芦醇可有效缓解大鼠力竭运动所致氧化应激状态,其机制可能与降低心肌组织Bax、caspase-3表达水平,减少心肌细胞凋亡有关。

Objective To explore protective effects of resveratrol （RIGS） on oxidative stress, carchomyocyte apoptosis in exercise-exhauted rats. Methods Fifty Sprague-Dawley （SD） specific pathogen-free （SPF） adult male rats were randomly divided into five groups （quiet control, exhaustive-exercise, and three RES treatment groups at the dosages of 50,100,200 mg/kg）. Superoxide dismutase （ SOD）, malondialdehyde （ MDA）, and calcium-activated adenosine triphosphatase （Ca2 ＋-ATPase） in heart tissues of all the rats were measured. Cell apoptosis was detected using terminal-deoxynucleotidyl transferase mediated nick end labeling （TUNEL） method. The expression of B cell lymyhoma/leukemia-2- associated X protein （Bax） and caspase-3 protein in the heart tissues were measured using Western blot. Results The myocardial tissues of exercise-exhausted rats showed significantly higher hypoxic-ischemic area （ 112. 27 ± 48.27 μm2 ）, cell apoptosis index （ 10. 4 ±1.3 ） % , MDA （ 3.98 ± 0. 75 nmol/mgpro）, Bax （ 1.28 ± 0. 32）, and caspase-3 （ 1.59 ± 0. 12） and lower SOD （30. 54 ± 4. 29 U/mgpro ）, Ca2 ＋ -ATPase （ 0. 32 ± 0.03 mol/mg . h） compared to those of the quiet control rats; the myocardial tissues of the rats treated with RES of 200 mg/kg manifested significantly lower hypoxic-ischemic area （22. 12 ± 10. 22 μm2 ）, cell apoptosis index （23.4 ± 2. 3 ） %, MDA （ 1.65 ± 0. 11 nmol/mgpro）, Bax （0. 36 ±0. 11） ,and caspase-3 （0. 62 ±0. 13） and higher SOD （69. 57 ±9.02 U/mgpro） ,Ca2＋ -ATPase （0. 72± 0. 11 mol/mg. h ） compared to those of the exercise-exhausted rats （ all P 〈 0.01 ）. Conclusion RES can reduce oxidative stress in exercise-exhausted rats and the effect may be related to the decreased Bax and caspase-3 expression in myocardial tissues and inhibited cardiomyocyte apoptosis.